In these studies the antiproliferative effects of methyl-prednisilone (MP) and dexamethasone (dex) were studied in a variety of experimental animal tumors. These models were the spontaneous mammary tumors in C3H/HeJ mice, their first generation transplants, S-180 ascites, T1699 mammary tumors, RIF tumors, Lewis lung, and two human tumor cell lines representative of human lung cancer growing as solid tumors in athymic nude mice. Our studies have shown that the antiproliferative effect of corticosteroids in these solid tumor models correlates closely with the level of specific cytoplasmic dex receptors as measured by competitive binding dextran charcoal assay and scatchard analysis. Our studies have also shown that MP and dex can induce reversible G1 progressive delay in experimental tumor models. Changes in the age distribution of G1 blocked cells after cessation of steroid treatments can be exploited to produce a better antitumor response to sequential chemotherapy with combinations of steroid, VCR and 5-FU.